Randomized Phase II Study of Temozolomide and Radiotherapy Compared With Radiotherapy Alone in Newly Diagnosed Glioblastoma Multiforme

Athanassiou, H.; Synodinou, M.; Maragoudakis, Evagelos; Paraskevaidis, M.; Verigos, C.; Misailidou, D.; Antonadou, D.; Saris, George; Beroukas, K.; Karageorgis, P.

doi:10.1200/jco.2005.00.331

Cited by 240 publications

(177 citation statements)

References 18 publications

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“…It can efficiently inhibit the proliferation of glioma cells and induce apoptosis. However, the action of TMZ on glioblastoma cells remains largely undefined, and glioblastomas are relatively resistant to the cytotoxic effects of TMZ (3). Recent findings support the existence of a stem cell-derived origin of gliomas (4).…”

Section: Introductionmentioning

confidence: 70%

MicroRNA-125b-2 confers human glioblastoma stem cells resistance to temozolomide through the mitochondrial pathway of apoptosis

et al. 2011

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Abstract. MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate protein expression by cleaving or repressing the translation of target mRNAs. miR-125b, one of the neuronal miRNAs, was recently found to be necessary for stem cell fission and for making stem cells insensitive to chemotherapy signals. Temozolomide (TMZ) is a promising chemotherapeutic agent for treating glioblastomas. However, resistance develops quickly and with a high frequency. Given the insensitivity of some glioblastomas to TMZ and the hypothesis that glioma stem cells cause resistance to drug therapy, exploring the functions and mechanisms of miR-125b action on TMZ-treated glioblastoma stem cells would be valuable. In this study, we found that miR-125b-2 is overexpressed in glioblastoma multiforme tissues and the corresponding stem cells (GBMSC); downregulation of miR-125b-2 expression in GBMSC could allow TMZ to induce GBMSC apoptosis. Additionally, the expression of the anti-apoptotic protein Bcl-2 was decreased after the TMZ+miR-125b-2 inhibitor treatment, while the expression of the proapoptotic protein Bax was increased. Further research demonstrated that the induction of apoptosis in GBMSC is also associated with increased cytochrome c release from mitochondria, induction of Apaf-1, activation of caspase-3 and poly-ADP-ribose polymerase (PARP). Taken together, these results suggest that miR-125b-2 overexpression might confer glioblastoma stem cells resistance to TMZ.

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Section: Introductionmentioning

confidence: 70%

MicroRNA-125b-2 confers human glioblastoma stem cells resistance to temozolomide through the mitochondrial pathway of apoptosis

et al. 2011

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“…However, that trial did not provide differential survival data regarding the methylation status of the MGMT gene promoter (24). Preliminary evidence indicates that the one week on/one week off TMZ schedule could also be active in patients with tumors lacking MGMT gene promoter methylation (6).…”

Section: Discussionmentioning

confidence: 99%

Chemoradiotherapy of Newly Diagnosed Glioblastoma With Intensified Temozolomide

Weiler

Hartmann

Wiewrodt³

et al. 2010

International Journal of Radiation Oncology*Biology*Physics

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“…The combined use of TMZ chemotherapy with radiotherapy after surgical resection has resulted in a statistically significant survival benefit for up to five years of follow up, compared with radiotherapy alone for the treatment of glioblastoma [3,4]. However, TMZ use is not without potential harmful effects.…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus pneumonitis following temozolomide for the treatment of glioblastoma multiforme

Bahrani¹,

Rotstein²

2017

Cancer Rep Rev

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Temozolomide (TMZ) is considered to be standard chemotherapy for the treatment of glioblastoma, but may cause lymphocytopenia thus potentiating the risk for opportunistic infections. Although one might anticipate that recurrent CMV infection may be precipitated by temozolomide immunosuppression, few cases of TMZ-induced cytomegalovirus (CMV) recurrent infection have been reported. Herein, we report a patient with malignant glioma who developed CMV pneumonia following TMZ therapy. The patient developed significant recurrent CMV infection with pneumonitis diagnosed by PCR (DNA analysis). Antiviral treatment with intravenous ganciclovir was administered. For patients with prior CMV exposure, it would be prudent to monitor CMV viral loads periodically to avoid recurrent CMV infection after exposure to TMZ and corticosteroid chemotherapy.

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Randomized Phase II Study of Temozolomide and Radiotherapy Compared With Radiotherapy Alone in Newly Diagnosed Glioblastoma Multiforme

Abstract: TMZ combined with RT (concomitantly and sequentially) seems to be more effective than RT alone in patients with newly diagnosed GBM. The combined-modality treatment was well tolerated.

Cited by 240 publications

References 18 publications

MicroRNA-125b-2 confers human glioblastoma stem cells resistance to temozolomide through the mitochondrial pathway of apoptosis

MicroRNA-125b-2 confers human glioblastoma stem cells resistance to temozolomide through the mitochondrial pathway of apoptosis

Chemoradiotherapy of Newly Diagnosed Glioblastoma With Intensified Temozolomide

Cytomegalovirus pneumonitis following temozolomide for the treatment of glioblastoma multiforme

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